Association of chronic obstructive pulmonary disease with coronary artery disease / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The relationship between chronic obstructive pulmonary disease (COPD) and coronary artery disease (CAD) remains largely unknown. This study aimed to explore the association of COPD with CAD, especially with multi-vessel disease (VD).</p><p><b>METHODS</b>The data of 354 patients who underwent multi-detector computed tomography (MDCT) for suspected CAD were analyzed. Luminal narrowing was defined as at least one lesion 50% or greater stenosis. The analysis of serum biochemistry profile and spirometry were performed on all eligible patients, and the diagnosis of COPD was defined as the criteria of Global Initiative for Chronic Obstructive Lung Disease.</p><p><b>RESULTS</b>Patients with CAD had a significantly higher complication of COPD than those without CAD (11.8% vs. 3.7%, P < 0.001). Comparing with patients without COPD, those with COPD were more likely to have multi-VD, proportion of smoking and high C-reactive protein (CRP) (P < 0.001). Multivariate Logistic regression analysis revealed that the multi-VD was significantly correlated with COPD (P=0.012) and CRP (P=0.015).</p><p><b>CONCLUSIONS</b>There was a high complication of COPD in patients with CAD, and COPD may be a critical risk factor for CAD, especially for multi-VD. CAD and COPD were closely associated and the interplay of systemic inflammation might in part explain the relationship between them.</p>

Relationship between 6-minute walk test and pulmonary function test in stable chronic obstructive pulmonary disease with different severities / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The relationship between the 6-minute walk test (6MWT) and pulmonary function test in stable chronic obstructive pulmonary disease (COPD) remains unclear. We evaluate the correlation of 6MWT and spirometric parameters in stable COPD with different severities. 6MWT data assessed included three variables: the 6-minute walk distance (6MWD), 6-minute walk work (6MWORK), and pulse oxygen desaturation rate (SPO(2)%).</p><p><b>METHODS</b>6MWT and pulmonary function test were assessed for 150 stable COPD patients with different severities. Means and standard deviations were calculated for the variables of interest. Analysis of variance was performed to compare means. Correlation coefficients were calculated for 6MWT data with the spirometric parameters and dyspnea Borg scale. Multiple stepwise regression analysis was used to screen pulmonary function-related predictors of 6MWT data.</p><p><b>RESULTS</b>The three variables of 6MWT all varied as the severities of the disease. The 6MWD and 6MWORK both correlated with some spirometric parameters (positive or negative correlation; the absolute value of r ranging from 0.34 to 0.67; P < 0.05) in severe and very severe patients, and the SPO2% correlated with the dyspnea Borg scale in four severities (r = -0.33, -0.34, -0.39, -0.53 respectively; P < 0.05). The 6MWD was correlated with the 6MWORK in four severities (r = 0.56, 0.57, 0.72, 0.81 respectively, P < 0.05), and neither of them correlated with the SPO(2)%. The percent of predicted forced expiratory volume in 1 second (FEV(1)% predicted) and residual volume to total lung capacity ratio (RV/TLC) were predictors of the 6MWD, and the maximum voluntary ventilation (MVV) was the predictor of the 6MWORK.</p><p><b>CONCLUSIONS</b>6MWT correlated with the spirometric parameters in severe and very severe COPD patients. 6MWT may be used to monitor changes of pulmonary function in these patients.</p>

Helicobacter pylori seroprevalence in patients with obstructive sleep apnea syndrome among a Chinese population

To investigate the seroprevalence of Helicobacter pylori [H. pylori] in patients with obstructive sleep apnea syndrome [OSAS], and to determine any association between H. pylori infection and severity of OSAS. Two hundred and forty-three subjects were recruited in this cross-sectional study at the Department of Respiratory Medicine in the West China Hospital, Sichuan, P. R. China, from October 2006 to April 2008. Polysomnography [PSG] was used to determine the apnea-hypopnea index [AHI], and enzyme-linked immunosorbent assay was used to test H. pylori IgG. According to the AHI, subjects were divided into 4 groups: the control group [AHI <5/hours], patients with mild OSAS group [AHI: 5-14/hours], moderate OSAS group [AHI: 15-29/hours], and severe OSAS group [AHI: >/= 30/hours]. The prevalence of H. pylori infection in patients with OSAS was 75.5%, and in the controls it was 53.4% [p=0.000]. The prevalence of H. pylori infection in patients with mild OSAS was 57.1%, with moderate OSAS was 76.5%, and with severe OSAS was 90.9%. There were significant differences between patients with moderate and severe OSAS and the controls, as well as among the mild, moderate, and severe OSAS groups. Helicobacter pylori infection may be associated with OSAS. In addition, increased severity of OSAS might be associated with higher seroprevalence of H. pylori

Simvastatin attenuates lipopolysaccharide-induced airway mucus hypersecretion in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Mucus hypersecretion in the respiratory tract and goblet cell metaplasia in the airway epithelium contribute to the morbidity and mortality associated with airway inflammatory diseases. This study aimed to examine the effect and mechanisms of simvastatin on airway mucus hypersecretion in rats treated with lipopolysaccharide (LPS).</p><p><b>METHODS</b>Mucus hypersecretion in rat airways was induced by intra-tracheal instillation of LPS. Rats treated with or without LPS were administered intra-peritoneally simvastatin (5 and 20 mg/kg) for 4 days. Expression of Muc5ac, RhoA and mitogen-activated protein kinases (MAPK) p38 in lung were detected by real-time polymerase chain reaction (PCR), immunohistochemistry or Western blotting. Tumor necrosis factor (TNF)-alpha and IL-8 in bronchoalveolar lavage fluid (BALF) were assayed by an enzyme-linked lectin assay and enzyme linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>Simvastatin attenuated LPS-induced goblet cell hyperplasia in bronchial epithelium and Muc5ac hypersecretion at both the gene and protein levels in lung (P <0.05). Moreover, simvastatin inhibited neutrophil accumulation and the increased concentration of TNF-alpha and IL-8 in BALF follows LPS stimulation (P < 0.05). The higher dose of simvastatin was associated with a more significant reduction in Muc5ac mRNA expression, neutrophil accumulation and inflammatory cytokine release. Simultaneously, the increased expression of RhoA and p38 MAPK were observed in LPS-treated lung (P <0.05). Simvastatin inhibited the expression of RhoA and p38 phosphorylation in lung following LPS stimulation (P < 0.05). However, the increased expression of p38 protein in LPS-treated lung was not affected by simvastatin administration.</p><p><b>CONCLUSIONS</b>Simvastatin attenuates airway mucus hypersecretion and pulmonary inflammatory damage induced by LPS. The inhibitory effect of simvastatin on airway mucus hypersecretion may be through, at least in part, the suppression of neutrophil accumulation and inflammatory cytokine release via inactivation of RhoA and p38 signaling pathway.</p>

Simvastatin attenuates bleomycin-induced pulmonary fibrosis in mice / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Bleomycin-induced fibrosis is extensively used to model aspects of the pathogenesis of interstitial pulmonary fibrosis. This study aimed to determine the benefic effects and mechanisms of simvastatin on bleomycin-induced pulmonary fibrosis in mice.</p><p><b>METHODS</b>Bleomycin-induced pulmonary fibrosis mice were administered with simvastatin in different doses for 28 days. We measured inflammatory response, fibrogenic cytokines and profibrogenic markers in both bleomycin-stimulated and control lungs, and correlated these parameters with pulmonary fibrosis.</p><p><b>RESULTS</b>Simvastatin attenuated the histopathological change of bleomycin-induced pulmonary fibrosis and prevented the increase of lung hydroxyproline content and collagen (I and III) mRNA expression induced by bleomycin. Moreover, simvastatin down-regulated the increased expression of transforming growth factor-beta1 (TGF-beta1) and connective tissue growth factor (CTGF) induced by bleomycin at both gene and protein levels. Simultaneously, the accumulation of neutrophils and lymphocytes and the increased production of tumor necrosis factor-alpha (TNF-alpha) in bronchial alveolar lavage fluid were inhibited by simvastatin in early inflammatory phase after bleomycin infusion. The higher dose of simvastatin was associated with a more significant reduction in these inflammatory and fibrotic parameters. Furthermore, the inactivation of p38, RhoA and Smad2/3 signaling pathways was observed during simvastatin administration.</p><p><b>CONCLUSIONS</b>Simvastatin attenuated bleomycin-induced pulmonary fibrosis, as indicated by decreases in Ashcroft score and lung collagen accumulation. The inhibitory effect of simvastatin on the progression of pulmonary fibrosis may be demonstrated by reducing inflammatory response and production of TGF-beta1 and CTGF. These findings indicate that simvastatin may be used in the treatment of pulmonary fibrosis.</p>

Increased expression of human calcium-activated chloride channel 1 is correlated with mucus overproduction in the airways of Chinese patients with chronic obstructive pulmonary disease / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Chronic obstructive pulmonary disease (COPD) is usually complicated with mucus overproduction in airway. Recently the increased expression of the human calcium-activated chloride channel 1 (CaCC(1)) was found to play an important role in mucus overproduction in the asthmatic airways. To investigate the relationship of CaCC(1) and mucus overproduction in the airway of Chinese patients with COPD, the expressions of CaCC(1), MUC5AC and mucus in bronchial tissues were examined.</p><p><b>METHODS</b>Bronchial tissues were obtained from fiberoptic bronchoscopy and bronchial biopsy in West China Hospital from April to July in 2004. Twenty-five patients were diagnosed as the patients with COPD overproduction, and other 20 were the control subjects. The expressions of CaCC(1), MUC5AC and mucin in bronchial tissues were detected by reverse transcriptase-polymerase chain reaction (RT-PCR), in situ hybridization with digoxigenin (DIG)-labeled RNA probe, immunohistochemical and alcian blue-periodic acid Schiff (AB-PAS) staining, respectively.</p><p><b>RESULTS</b>Compared with the control group, the stronger expressions of CaCC(1) were further detected throughout the bronchial tissues from patients with COPD (P < 0.01). Furthermore, the stronger expressions of the CaCC(1) mRNA were related to the severity of airflow obstruction. Samples from COPD showed a stronger staining for MUC5AC than those in control subjects (P < 0.01) and AB-PAS staining revealed more mucins in COPD patients' submucosal gland comparing with that in control subjects (P < 0.01). Expression levels of the CaCC(1) mRNA were respectively negatively correlated with the patients' forced expiratory volume in one second (FEV(1))/forced vital capacity (FVC) data, FEV(1)% predicted data, V(50)% predicted data, V(25)% predicted data (r = -0.43, r = -0.43, r = -0.35, r = -0.36, P < 0.01, P < 0.01, P < 0.05, P < 0.05). While the expression levels of the CaCC(1) mRNA were well correlated with the expression levels of the MUC5AC mRNA of airway epithelium and the PAS-AB stained area of submucosal glands (r = 0.39, r = 0.46, P < 0.05, P < 0.01). Expression levels of the MUC5AC mRNA were negatively correlated with the patients' FEV(1)/FVC data (P = 0.01), FEV(1)% pred data (P = 0.01), V(50)% predicted data, V(25)% predicted data (r = -0.53, r = -0.53, r = -0.48, r = -0.43, P < 0.01, P < 0.01, P < 0.01, P < 0.01). While the expression levels of the MUC5AC mRNA were well correlated with the positively PAS-AB stained area of submucosal gland (P < 0.05), and the correlation coefficients were 0.43.</p><p><b>CONCLUSION</b>These results suggest that the stronger gene expression of CaCC(1) exists, complicated with mucus overproduction in the airway of Chinese patients with COPD.</p>